James H. Catterson

This study establishes an adult-onset Drosophila model of tauopathy, revealing sex-specific effects on survival and behavior and identifying genetic modifiers of tau-induced dysfunction.

This study uses live human brain slice cultures to show that physiological and pathological amyloid-beta have opposing effects on synapses, with physiological levels enhancing synaptic transcripts and pathological levels causing synaptic loss.

This study shows that inhibiting S6K in Drosophila and mice reduces age-related inflammation and extends lifespan through the endolysosomal system and immune pathways.

The paper identifies transmembrane protein 97 as a synaptic receptor for amyloid beta in human Alzheimer's disease using advanced microscopy and drug intervention studies.

The paper shows Drosophila melanogaster resist trans-synaptic spread of human tau, suggesting they are not suitable for screening tau propagation modifiers.

This study shows that retaining proteins in the ER can rescue Aβ toxicity in Drosophila and mouse models, suggesting a potential therapeutic strategy for Alzheimer's disease.